Together with the immunohistochemical results on clinical specimens of our medulloblastoma cohort, the findings of enhanced 53BP1 bodies and hence endogenous replication stress in the medulloblastoma cell lines raised the question whether HCMV infection might in any way impact the extent of replication stress and/or the formation of the 53BP1 bodies. This evidence concerns the gene TP53BP1 and cytomegalovirus infection.